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Epilogue
Published in Ulrik Kihlbom, Mats G. Hansson, Silke Schicktanz, Ethical, Social and Psychological Impacts of Genomic Risk Communication, 2020
Mats G. Hansson, Ulrik Kihlbom, Silke Schicktanz
Barker explained the concept of foetal growth affecting adult disease in two seminal papers (Barker 1992; Barker 1995). Numerous studies have since then been carried out in order to investigate the effects of early dietary exposure on adult health. Health records collected during the Dutch Hunger Winter of 1944–1945 allowed analysis of long-term consequences of prenatal famine (Stuffrein-Roberts et al. 2008). An association was found between severe nutritional deficiency and schizophrenia (Susser et al. 1996). The relationship was replicated by analysis of health records of the famine in China during 1959–1961 (St Clair et al. 2005). There remain considerable gaps in the knowledge of causal relationships between perinatal nutrition and health endpoints at later stages in life through epigenetic mechanisms, and there may be many confounders that must be identified and controlled for, but evidence on metabolic imprinting/programming is building up rapidly (Hanley et al. 2010). Recent studies point also to a relationship between early life precursors, epigenetics and food allergy (Hong and Wang 2012).
The metabolic basis of obesity
Published in Anna Bellisari, The Anthropology Of Obesity in the United States, 2016
No time is more important than the prenatal and early postnatal stages in the development of human physiology. The fetus is, of course, dependent on its mother for nourishment, so both maternal under-nutrition and over-nutrition leave their mark on an infant’s developing metabolic system, and both may predispose to obesity throughout the rest of life. Metabolic imprinting during early development permanently fixes neural circuits and functions, and also establishes the expression of genes associated with appetite and energy metabolism for a lifetime. As noted in examples below, the remarkable human capacity to adjust to nutritional restriction during pre- and postnatal life stages helps to ensure the survival of the individual and the species, but at the price of potential obesity and associated health problems (such as diabetes) in later life. This trade-off in early development – sacrificing health for survival – is irreversible (Wells 2013).
Nutritional stress timing differentially programs cognitive abilities in young adult male mice
Published in Nutritional Neuroscience, 2022
Bruno G. Berardino, Fabricio Ballarini, Mariela Chertoff, Lionel M. Igaz, Eduardo T. Cánepa
In this work, mice were subjected to a low-protein isocaloric diet from gestation to weaning or from weaning to the end of adolescence for a matched-duration period. As we have previously shown, protein restriction during gestation and lactation renders pups with a significant deficit in body weight at weaning even after the nutritional recovery period, remaining 12% lighter than control mice ([24] and Figure 2). This result agrees with those obtained in other studies which reported a persistent reduction in the body weight of rodents subjected to protein malnutrition [34,35]. Conversely, malnutrition during adolescence did not cause a significant change in body weight. Epidemiological data suggest that the nutritional condition of the mother can influence the body weight of the offspring by means of metabolic imprinting [36]. In particular, protein-deficient diets have been involved as important regulators of metabolic programming and later health outcomes in rodents [23]. In this regard, our results support previous hypotheses arguing that, in adult animals, the regulation of body weight is determined during gestation and lactation and, therefore, the body weight of adults would depend on the nutritional conditions imposed during these periods [37].
Undernutrition – thirty years of the Regional Basic Diet: the legacy of Naíde Teodósio in different fields of knowledge
Published in Nutritional Neuroscience, 2022
Larissa B. Jannuzzi, Amaury Pereira-Acacio, Bruna S. N. Ferreira, Debora Silva-Pereira, João P. M. Veloso-Santos, Danilo S. Alves-Bezerra, Jarlene A. Lopes, Glória Costa-Sarmento, Lucienne S. Lara, Leucio D. Vieira, Ricardo Abadie-Guedes, Rubem C.A. Guedes, Adalberto Vieyra, Humberto Muzi-Filho
Regarding the reproductive system, the RBD feeding in pregnant rats decreased the number of pups per litter, with low weight gain during gestation. In addition, RBD caused a low body weight at birth, together with marked post-weaning immaturity and high mortality rates, occurring in 3 consecutive rat generations [68]. This gave important proof of the idea that metabolic imprinting during gestation can be passed on from generation to generation.